Dataset Information

Troponin elevation in acute ischemic stroke (TRELAS)--protocol of a prospective observational trial.

ABSTRACT: Levels of the cardiac muscle regulatory protein troponin T (cTnT) are frequently elevated in patients with acute ischemic stroke and elevated cTnT predicts poor outcome and mortality. The pathomechanism of troponin release may relate to co-morbid coronary artery disease and myocardial ischemia or, alternatively, to neurogenic cardiac damage due to autonomic activation after acute ischemic stroke. Therefore, there is uncertainty about how acute ischemic stroke patients with increased cTnT levels should be managed regarding diagnostic and therapeutic workup.The primary objective of the prospective observational trial TRELAS (TRoponin ELevation in Acute ischemic Stroke) is to investigate the frequency and underlying pathomechanism of cTnT elevation in acute ischemic stroke patients in order to give guidance for clinical practice. All consecutive patients with acute ischemic stroke admitted within 72 hours after symptom onset to the Department of Neurology at the Campus Benjamin Franklin of the University Hospital Charité will be screened for cTnT elevations (i.e. ? 0.05 ?g/l) on admission and again on the following day. Patients with increased cTnT will undergo coronary angiography within 72 hours. Diagnostic findings of coronary angiograms will be compared with age- and gender-matched patients presenting with Non-ST-Elevation myocardial infarction to the Department of Cardiology. The primary endpoint of the study will be the occurrence of culprit lesions in the coronary angiogram indicating underlying co-morbid obstructive coronary artery disease. Secondary endpoints will be the localization of stroke in the cerebral imaging and left ventriculographic findings of wall motion abnormalities suggestive of stroke-induced global cardiac dysfunction.TRELAS will prospectively determine the frequency and possible etiology of troponin elevation in a large cohort of ischemic stroke patients. The findings are expected to contribute to clarify pathophysiologic concepts of co-morbid cardiac damage in ischemic stroke patients and also to provide a basis for clinical recommendations for cardiac workup of such patients.clinicaltrials.gov NCT01263964.

SUBMITTER: Scheitz JF

PROVIDER: S-EPMC3166899 | biostudies-literature | 2011 Aug

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Troponin elevation in acute ischemic stroke (TRELAS)--protocol of a prospective observational trial.

Scheitz Jan F JF Mochmann Hans-Christian HC Nolte Christian H CH Haeusler Karl G KG Audebert Heinrich J HJ Heuschmann Peter U PU Laufs Ulrich U Witzenbichler Bernhard B Schultheiss Heinz-Peter HP Endres Matthias M

BMC neurology 20110808

<h4>Background</h4>Levels of the cardiac muscle regulatory protein troponin T (cTnT) are frequently elevated in patients with acute ischemic stroke and elevated cTnT predicts poor outcome and mortality. The pathomechanism of troponin release may relate to co-morbid coronary artery disease and myocardial ischemia or, alternatively, to neurogenic cardiac damage due to autonomic activation after acute ischemic stroke. Therefore, there is uncertainty about how acute ischemic stroke patients with inc ...[more]

PMID: 21824425

Similar Datasets

Project description:Background. Cardiac morbidities account for 20% of deaths after ischemic stroke and is the second commonest cause of death in acute stroke population. Elevation of cardiac troponin has been regarded as a prognostic biomarker of poor outcome in patients with acute stroke. Methods. This retrospective study enrolled 871 patients with acute ischemic stroke from August 2010 to March 2015. Data included vital signs, laboratory parameters collected in the emergency department, and clinical features during hospitalization. National Institutes of Health Stroke Scale (NIHSS), Barthel index, and modified Rankin Scale (mRS) were used to assess stroke severity and outcome. Results. Elevated troponin I (TnI) > 0.01 µg/L was observed in 146 (16.8%) patients. Comparing to patients with normal TnI, patients with elevated TnI were older (median age 77.6 years vs. 73.8 years), had higher median heart rates (80 bpm vs. 78 bpm), higher median white blood cells (8.40 vs. 7.50 1,000/m(3)) and creatinine levels (1.40 mg/dL vs. 1.10 mg/dL), lower median hemoglobin (13.0 g/dL vs. 13.7 g/dL) and hematocrit (39% vs. 40%) levels, higher median NIHSS scores on admission (11 vs. 4) and at discharge (8 vs. 3), higher median mRS scores (4 vs3) but lower Barthel index scores (20 vs. 75) at discharge (p < 0.001). Multivariate analysis revealed that age ≥ 76 years (OR 2.25, CI [1.59-3.18]), heart rate ≥ 82 bpm (OR 1.47, CI [1.05-2.05]), evidence of clinical deterioration (OR 9.45, CI [4.27-20.94]), NIHSS score ≥ 12 on admission (OR 19.52, CI [9.59-39.73]), and abnormal TnI (OR 1.98, CI [1.18-3.33]) were associated with poor outcome. Significant factors for in-hospital mortality included male gender (OR 3.69, CI [1.45-9.44]), evidence of clinical deterioration (OR 10.78, CI [4.59-25.33]), NIHSS score ≥ 12 on admission (OR 8.08, CI [3.04-21.48]), and elevated TnI level (OR 5.59, CI [2.36-13.27]). C-statistics revealed that abnormal TnI improved the predictive power of both poor outcome and in-hospital mortality. Addition of TnI > 0.01 ug/L or TnI > 0.1 ug/L to the model-fitting significantly improved c-statistics for in-hospital mortality from 0.887 to 0.926 (p = 0.019) and 0.927 (p = 0.028), respectively. Discussion. Elevation of TnI during acute stroke is a strong independent predictor for both poor outcome and in-hospital mortality. Careful investigation of possible concomitant cardiac disorders is warranted for patients with abnormal troponin levels.

Project description:BackgroundElevated cardiac troponin, which indicates cardiomyocyte injury, is common after acute ischemic stroke and is associated with poor functional outcome. Myocardial injury is part of a broad spectrum of cardiac complications that may occur after acute ischemic stroke. Previous studies have shown that in most patients, the underlying mechanism of stroke-associated myocardial injury may not be a concomitant acute coronary syndrome. Evidence from animal research and clinical and neuroimaging studies suggest that functional and structural alterations in the central autonomic network leading to stress-mediated neurocardiogenic injury may be a key underlying mechanism (ie, stroke-heart syndrome). However, the exact pathophysiological cascade remains unclear, and the diagnostic and therapeutic implications are unknown.ObjectiveThe aim of this CORONA-IS (Cardiomyocyte injury following Acute Ischemic Stroke) study is to quantify autonomic dysfunction and to decipher downstream cardiac mechanisms leading to myocardial injury after acute ischemic stroke.MethodsIn this prospective, observational, single-center cohort study, 300 patients with acute ischemic stroke, confirmed via cerebral magnetic resonance imaging (MRI) and presenting within 48 hours of symptom onset, will be recruited during in-hospital stay. On the basis of high-sensitivity cardiac troponin levels and corresponding to the fourth universal definition of myocardial infarction, 3 groups are defined (ie, no myocardial injury [no cardiac troponin elevation], chronic myocardial injury [stable elevation], and acute myocardial injury [dynamic rise/fall pattern]). Each group will include approximately 100 patients. Study patients will receive routine diagnostic care. In addition, they will receive 3 Tesla cardiovascular MRI and transthoracic echocardiography within 5 days of symptom onset to provide myocardial tissue characterization and assess cardiac function, 20-min high-resolution electrocardiogram for analysis of cardiac autonomic function, and extensive biobanking. A follow-up for cardiovascular events will be conducted 3 and 12 months after inclusion.ResultsAfter a 4-month pilot phase, recruitment began in April 2019. We estimate a recruitment period of approximately 3 years to include 300 patients with a complete cardiovascular MRI protocol.ConclusionsStroke-associated myocardial injury is a common and relevant complication. Our study has the potential to provide a better mechanistic understanding of heart and brain interactions in the setting of acute stroke. Thus, it is essential to develop algorithms for recognizing patients at risk and to refine diagnostic and therapeutic procedures.Trial registrationClinicaltrials.gov NCT03892226; https://www.clinicaltrials.gov/ct2/show/NCT03892226.International registered report identifier (irrid)DERR1-10.2196/24186.

Project description:IntroductionIt is unknown which comorbidities and stroke characteristics are associated with elevated cardiac troponin (cTn) levels after stroke. The main objective of this systematic review and meta-analysis is to assess the association of elevated cTn with preexisting cardiovascular comorbidities (eg, coronary artery disease, heart failure and structural heart disease), specific stroke characteristics (eg, infarct/haemorrhage size, stroke severity, insular cortex involvement) and renal failure after ischaemic stroke (IS) or intracranial haemorrhage (ICH). The secondary objective is to evaluate the association of elevated cTn with stroke recurrence and death.Methods and analysisWe will include all cross-sectional, case-control, cohort studies and clinical trials involving IS and ICH adult patients (≥18 years), published between 1 January 1990 and 31 December 2020 in English or Spanish, reporting the proportion with elevated cTn. We will search PubMed, EMBASE and Web of Science by applying predefined search terms. Two reviewers will independently screen titles and abstracts, retrieve full texts, extract the data in a predesigned form, and assess the risk of bias. We will apply random-effects or fixed-effects meta-analyses to estimate the association between cardiovascular comorbidities, stroke characteristics and renal failure with cTn elevation. We will report results as risk ratios or ORs. We will perform sensitivity analyses for subtypes of cTn (cTn-I and cTn-T), regular versus high-sensitivity assays, and type of stroke (IS vs ICH). We will estimate heterogeneity by using t2 Q and I2 measures. We will use funnel plots, Rosenthal's Fail-Safe N, Duval and Tweedie's trim and fill procedure, and Egger's regression intercept to assess publication bias.Ethics and disseminationThis review will be based on published data and does therefore not require ethical clearance. The results will be published in peer-reviewed journals.Prospero registration numberCRD42020203126.

Project description:ObjectivesAspiration after stroke has been associated with aspiration pneumonia, which contributes to increased mortality of stroke. Laryngeal elevation is a core mechanism for protection from aspiration. Few studies have explored the predictive value of laryngeal elevation velocity for aspiration after stroke. This study aimed to explore the ability of laryngeal elevation velocity to predict aspiration in patients with acute ischemic stroke.MethodsThis was a prospective cohort study that included consecutive acute ischemic stroke patients treated at a teaching hospital during a 10-month period. Patients underwent magnetic resonance imaging (MRI) to confirm the diagnosis of acute ischemic stroke. Patients who were at risk of aspiration and could swallow 5 ml of diluted barium (40%, w/v) for a videofluoroscopic swallowing (VFS) study were included. The association between abnormal indices in the oral and pharyngeal phase of the VFS study and aspiration was examined using univariate analyses. These indices included the lip closure, tongue movement and control, laryngeal elevation velocity and range, the latency of pharyngeal swallowing, pharyngeal transit time (PTT), abnormal epiglottis tilt, residual barium in the pharynx, and the duration of upper esophageal sphincter (UES) opening. The laryngeal elevation velocity (%/s) was calculated as the range of laryngeal elevation (%) from the resting position to the maximum superior position or to the position where the laryngeal vestibule is fully closed divided by the corresponding duration of laryngeal elevation. The range of laryngeal elevation (%) was the percentage calculated as the distance between the resting laryngeal position and the maximum superior excursion position or position where the laryngeal vestibule is fully closed divided by the distance between the resting laryngeal position and the lowest edge of the mandible. A logistic regression analysis was used to determine the predictive value for aspiration secondary to reduced laryngeal elevation velocity after adjusting for the effects of other indices. Intrarater and interrater reliability were calculated using Pearson's correlation coefficients.ResultsData from 89 patients were analyzed. This cohort included 71 males and 18 females with a mean age of 59.31±11.46 years. The mean time from stroke onset to the VFS study was 3 days (1-7). Twenty one (23%) patients aspirated while swallowing 5 ml of diluted barium (40%, w/v). Aspiration was associated with age, the velocity (%/s) of laryngeal elevation and duration, delayed pharyngeal phase, pharyngeal transit time, abnormal epiglottic tilt, and invalid laryngeal elevation before true swallowing, and duration of upper esophageal sphincter (UES) opening. After adjusting for the effects of the indices mentioned above, logistic regression analysis revealed that a reduced of laryngeal elevation velocity before vestibule closure was predictive of aspiration independently (OR, 0.993; 95% CI, 0.987-1.000).DiscussionsReduced laryngeal elevation velocity for laryngeal elevated to position where laryngeal vestibule is fully closed was an independent predictor of aspiration in patients with acute ischemic stroke. This may be related to a decreased contraction velocity of the muscles involved in hyolaryngeal elevation. Therapeutic methods aimed at improving laryngeal elevation velocity may decrease aspiration events and pneumonias after stroke.

Dataset Information

Troponin elevation in acute ischemic stroke (TRELAS)--protocol of a prospective observational trial.

Publications

Troponin elevation in acute ischemic stroke (TRELAS)--protocol of a prospective observational trial.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets